Skip to main content
. Author manuscript; available in PMC: 2018 Mar 29.
Published in final edited form as: Nat Commun. 2013;4:2436. doi: 10.1038/ncomms3436

Figure 4. PMN bearing ITIM–SIRPα have enhanced peritoneal infiltration and IL-17 promotes ITIM–SIRPα formation.

Figure 4

(a) Control mice (water) and mice treated with DSS for various days were injected with 0.5 mg zymosan A followed by analyses of PMN infiltration into the peritoneum at different time points. (b) Mice with/without STZ treatment were injected with zymosan A followed by analysis of PMN migration into the peritoneum at 2 h. The results in a are presented as means±s.d., representing three to five independent experiments with multiple mice per group. *P<0.05; **P<0.01 as assessed by Student’s t-test. (c,d) IL-17 treatment (20 μg IL-17A, intravenously every other day for a total of three times) resulted in the loss of SIRPα cytoplasmic ITIMs in mouse bone marrow PMN. The data are presented as means±s.d., **P<0.01 determined by Student’s t-test. (e) Inhibition of IL-17 by the administration of an anti-mouse IL-17A antibody (50 μg, intravenously) on days 6 and 9 during DSS treatment. Anti-IL-17A antibody administration prevented the cleavage of SIRPα cytoplasmic ITIMs in PMNs (f,g) and abolished the enhancement of PMN infiltration during DSS treatment (h). The results are presented as means±s.d. and represent three independent experiments with three to five mice per condition. *P<0.05; **P<0.01 as assessed by Student’s t-test.